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SURGERY > WOUND HEALING > Flashcards

WOUND HEALING Flashcards

1
Q

Precedes and initiates inflammation with the ensuing release of chemotactic factors from the wound site.

A

Hemostasis

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2
Q

The first infiltrating cells to enter the wound site, peaking at 24-48 hours. Primary role of this is phagocytodis of bacteria and tissue. debris

A

PMN

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3
Q

The 2nd population of inflammatory cells that invades the wound. Achieve significant numbers in the wound by 48-96hrs post injury and remain present until wound healing is complete. Central function is activation and recruitment of other cells via mediators such as cytokines and growth factors.

A

Macrophages

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4
Q

Peak at 1 week post injury and truly bridge the transition from the inflammatory to the proliferative phase of healing. Plays an active role in the modulation of the wound environment.

A

Lymphocytes

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5
Q

Next phase to hemostasis and inflammation which spans 4 through 12 days. Fibroblasts and endothelial cells are the last cell populations to infiltrate the healing wound.

A

Proliferates

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6
Q

TThe strongest chemotactic factor for fibroblasts is

A

PDGF

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7
Q

Proliferate extensively or participate in angiogenesis)

A

Endothelial cells

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8
Q

The most abundant protein in the body

A

Collagen

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9
Q

The major component of extracellular matrix of the skin

A

Type I collagen

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10
Q

Type of collagen becomes more important during the repair process

A

TYpe III

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11
Q

Comprise a large portion of the “ground substance” that makes up granulation tissue. The major types present in wounds are dermatan and chondroitin sulfate

A

Glycosaminoglycans

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12
Q

Begins during the fibroplastic phasae and is characterized by a reorganization of previously synthesized collagen

A

Maturation and Remodeling

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13
Q

Pattern of desposition of matrix:

A
  • Fobronectin and collagen type III constitute the early matrix scaffolding
  • Glycosaminoglycans represent the next significant matrix components
  • Collagen type I is the final matrix
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14
Q

The final step in establishing tissue integrity. It is characterized primarily by proliferation and migration of epithelial cells adjacent to the wound.

A

Epithelization

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15
Q

All wounds undergo some degree of this. For wounds that do not have surgically appx. edged, the area of the wound will be decreased by this action.

A

Wound Contraction

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16
Q

Postulated as the major cell responsible for contraction. It differs from the normal fibroblast in that it possesses a cytoskeletal structure

A

Myofibroblast

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17
Q

Types of Ehlers - Danlos Syndrome:

Skin: thin, translucent, visiblr veins, normal scarring, no hyperentennsibility; no joint hypermobility; arterial, bowel and uterin rupture. Type III collagen defect.

A

Type IV

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18
Q

Types of Ehlers - Danlos Syndrome:

Skin: sofy, hyperextensible, easily bruising, fragile, atrophic scars; hypermobile joints; varicose veins; premature births

A

Type I

19
Q

Types of Ehlers - Danlos Syndrome:

Similar to Type II but inheritance is XLR

A

Type V

20
Q

Types of Ehlers - Danlos Syndrome:

Similar to Type I, but less severe

A

Type II

21
Q

Types of Ehlers - Danlos Syndrome:

SKin: soft, not hyperextensible, normal scars; small and large joint hypermobility

A

Type III

22
Q

Types of Ehlers - Danlos Syndrome:

Hypermobile joints, skin fragility. Absence of tenasein X protein.

A

TNx

23
Q

Types of Ehlers - Danlos Syndrome:

Similar to Type II with abnormal clotting studies. Fibronectin defect.

A

Type X

24
Q

Types of Ehlers - Danlos Syndrome:

Skin: soft, ;ax; bladder diverticula and rupture; limited pronation and supination; broad clavicle; occipital horns. Lysyl oxidase defect with abnormal copper use.

A

Type IX

25
Q

Types of Ehlers - Danlos Syndrome:

Skin: soft, hyperextensible, easy bruising, abnormal scars with purple discoloration, hypermobile joints; generalized periodontitis

A

Type VIII

26
Q

Types of Ehlers - Danlos Syndrome:

Skin: soft, mild hyperextensibility, no increased fragility; extremely lax joints with discolorations. Type I collagen gene defect.

A

Type VII

27
Q

Types of Ehlers - Danlos Syndrome:

Skin; hyperextensible, fragile, easy bruising; hypermobile joints; hypotonia, kyphoscoliosis. Lysyl hydroxylase deficiency

A

Type VI

28
Q

Tall stature, arachnodactyly, lax ligaments, myopia, scoliosis, pectus excavatum, and aneurysm of the ascending aorta. They are prone to hernias. Hyperextensible skin but shows no delay in wound healing. A mutation in the FBN1 gene

A

Marfan Sydrome

29
Q

Type of Osteogenesis Imperfecta:

Mild to moderate bone fragility; normal or gray sclera; mild short stature

A

Type IV

30
Q

Type of Osteogenesis Imperfecta:

“Prenatal lethal”; crumpled long bones, thin ribs, dark blue sclera

A

Type II

31
Q

Type of Osteogenesis Imperfecta:

Progressively deforming; multiple fractures; early loss of ambulation

A

Type III

32
Q

Type of Osteogenesis Imperfecta:

Mild bone fragility, blue sclera

A

Type I

33
Q

GI Tract VS Skin

pH: Varies throughout GI tract in accordance with local exocrine secretions

Microorganisms: Aerobic and anaerobic, especially in the colon and rectum; problamatic if they contaminate the peritoneal cavity

Shear stress: Intraluminal bulk transit and peristalsis exert distracting forces on the anastomosis

Tissue Oxygenation: Depedendent on intact vascular supply and neocapillary formation

A

GI Tract

34
Q

GI Tract VS Skin

pH: Usually constant except during sepsis or local infection

Microorganisms: Commensals rarely cause problems

Shear stress: Skeletal movements may stress the suture line but pain usually acts as a protective mechanism preventing excess movement

Tissue Oxygenation: Circulatory transport of oxugen as well as diffusion

A

Skin

35
Q

GI layer with greatest suture holding capacity

A

Submucosa

36
Q

GI layer that water tight seal from the luminal side of the bowel

A

Serosa

37
Q

GI layer that imparts the greates tensile strength

A

Submucosa

38
Q

Healing Process in Bone

A
  1. Accumulation of blood at the fracture site
  2. Liquefaction and degradation of nonviable products at the fracture site
  3. Soft callus stage
  4. Hard callus stage
  5. Remodelling phase
39
Q

There is disruption of proteoglycan matrix and injury to the chondrocytes. They are slow to heal and often result in persistent structural defect

A

Superficial injury

40
Q

Involve the underlying bone and soft tissue. Exposure of vascular channels of the surrounding damaged tissue that may help in the formation of granulation tissue

A

Deep injuries

41
Q

Matrix is characterized by accumulation of Type I and III collagen along with increased water, DNA, and glycosaminoglycan content. Restoration of the mechanical integrity may never be equal to that of tyhe undamaged tendon

A

Healing in Tendon

42
Q

Specialized cells, are metabolically very active and retain a large regenerative potential even in the absence of vascularity

A

Tenocytes

43
Q

Classification of WOund that healing is not achieved after 4 weeks of treatment

A

Chronic

SURGERY (9 decks)

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